ABSTRACT
In the aquatic environment, the primary pollutants of heavy metals and pharmaceuticals always occur in coexisting forms, and the research about combined impacts remains unclear, especially transgenerational effects. Cadmium (Cd) is a heavy metal that can damage the endocrine reproduction systems and cause thyroid dysfunction in fish. Meanwhile, ketoprofen (KPF) is a nonsteroidal anti-inflammatory drug (NSAID) that can cause neurobehavioral damage and physiological impairment. However, to our knowledge, the combined exposure of Cd and KPF in transgenerational studies has not been reported. In this investigation, sexually mature zebrafish were subjected to isolated exposure and combined exposure to Cd (10 µg/L) and KPF (10 and 100 µg/L) at environmentally relevant concentrations for 42 days. In this background, breeding capacity, chemical accumulation rate in gonads, and tissue morphologies are investigated in parental fish. This is followed by examining the malformation rate, inflammation rate, and gene transcription in the F1 offspring. Our results indicate that combined exposure of Cd and KPF to the parental fish could increase the chemical accumulation rate and tissue damage in the gonads of fish and significantly reduce the breeding ability. Furthermore, these negative impacts were transmitted to its produced F1 embryos, reflected by hatching rate, body deformities, and thyroid axis-related gene transcription. These findings provide further insights into the harm posed by Cd in the presence of KPF to the aquatic ecosystems.
ABSTRACT
Indole-3-acetic acid (IAA), a protein-bound uremic toxin, has been linked to cardiovascular morbidity and mortality in chronic kidney disease (CKD) patients. This study explores the influence of IAA (125 mg/kg) on cardiovascular changes in adenine sulfate-induced CKD rats. HPLC analysis revealed that IAA-exposed CKD rats had lower excretion and increased circulation of IAA compared to both CKD and IAA control groups. Moreover, echocardiography indicated that CKD rats exposed to IAA exhibited heart enlargement, thickening of the myocardium, and cardiac hypertrophy in contrast to CKD or IAA control group. Biochemical analyses supported the finding that IAA-induced CKD rats had elevated serum levels of c-Tn-I, CK-MB, and LDH; there was also evidence of oxidative stress in cardiac tissues, with a significant decrease in SOD and CAT levels, as well as an increase in MDA levels. The gene expression analysis found significant increases in ANP, BNP, ß-MHC, TNF-α, IL-1ß, and NF-κB levels in IAA-exposed CKD groups in contrast to the CKD or IAA control group. In addition, higher cardiac fibrosis markers, including Col-I and Col-III. The findings of this study indicate that IAA could trigger cardiovascular inflammation and fibrosis in CKD conditions.
ABSTRACT
The prevalent use of Azorubine (E122) and the unintentional food additive, Bisphenol A (BPA), in ready-to-drink (RTD) beverages raises significant health concerns, especially for children. The combined impact on embryonic development must be explored despite individual safety assessments. Our investigation revealed that the combined exposure of E122 and BPA at beverage concentration significantly induces mortality and morphological deformities, including reduced growth, pericardial edema, and yolk sac edema. The co-exposure triggers oxidative stress, impairing antioxidant enzyme responses and resulting in lipid and cellular damage. Notably, apoptotic cells are observed in the neural tube and notochord of the co-exposed larvae. Critical genes related to the antioxidant response elements (nrf2, ho1, and nqo1), apoptosis activation (bcl2, bax, and p53), and pro/anti-inflammatory cytokines (nfkb, tnfa, il1b, tgfb, il10, and il12) displayed substantial changes, highlighting the molecular mechanisms. Behavior studies indicated hypo-locomotion with reduced thigmotaxis and touch response in co-exposed larvae, distinguishing it from individual exposures. These findings underscore the neurodevelopmental impacts of E122 and BPA at reported beverage concentrations, emphasizing the urgent need for comprehensive safety assessments, particularly for child consumption.
ABSTRACT
The growing concern about pollution and toxicity in aquatic as well as terrestrial organisms is predominantly caused due to waterborne exposure and poses a risk to environmental systems and human health. This study addresses the co-toxic effects of cadmium (Cd) and ketoprofen (KPF), representing heavy metal and pharmaceutical discharge pollutants, respectively, in aquatic ecosystems. A 96-h acute toxicity assessment was conducted using zebrafish embryos. The results indicated that high dosages of KPF (10, 15, and 100 µg/mL) and Cd (10 and 15 µg/mL) reduced survivability and caused concentration-dependent deformities such as scoliosis and yolk sac edema. These findings highlight the potential defects in development and metabolism, as evidenced by hemolysis tests demonstrating dose-dependent effects on blood cell integrity. Furthermore, this study employs adult zebrafish for a 42-day chronic exposure to Cd and KPF (10 and 100 µg/L) alone or combined (10 + 10 and 100 + 100 µg/L) to assess organ-specific Cd and KPF accumulation in tissue samples. Organ-specific accumulation patterns underscore complex interactions impacting respiratory, metabolic, and detoxification functions. Prolonged exposure induces reactive oxygen species formation, compromising antioxidant defense systems. Histological examinations reveal structural changes in gills, gastrointestinal, kidney, and liver tissues, suggesting impairments in respiratory, osmoregulatory, nutritional, and immune functions. This study emphasizes the importance of conducting extensive research on co-toxic effects to assist with environmental risk assessments and safeguard human health and aquatic ecosystems.
ABSTRACT
Plant growth regulators (PGRs) are increasingly used to promote sustainable agriculture, but their unregulated use raises concerns about potential environmental risks. Indole-3-acetic acid (IAA), a commonly used PGR, has been the subject of research on its developmental toxicity in the in-vivo zebrafish model. IAA exposure to zebrafish embryos caused oxidative stress, lipid peroxidation, and cellular apoptosis. The study also revealed that critical antioxidant genes including sod, cat, and bcl2 were downregulated, while pro-apoptotic genes such as bax and p53 were upregulated. IAA exposure also hampered normal cardiogenesis by downregulating myl7, amhc, and vmhc genes and potentially influencing zebrafish neurobehavior. The accumulation of IAA was confirmed by HPLC analysis of IAA-exposed zebrafish tissues. These findings underscore the need for further study on the potential ecological consequences of IAA use and the need for sustainable agricultural practices.
Subject(s)
Down-Regulation , Embryo, Nonmammalian , Indoleacetic Acids , Oxidative Stress , Zebrafish , Animals , Oxidative Stress/drug effects , Down-Regulation/drug effects , Embryo, Nonmammalian/drug effects , Heart/drug effects , Apoptosis/drug effects , Plant Growth Regulators/toxicity , Lipid Peroxidation/drug effects , Zebrafish Proteins/genetics , Zebrafish Proteins/metabolismABSTRACT
A novel colorimetric and fluorogenic probe L based on hydrazine carbothioamide and 1,8-naphthalimide moieties has been designed and synthesized for the hypersensitive detection of Hg2+ or Ag+ ions. The observed probe L showed colorimetric and fluorometric responses for these studies when Hg2+ or Ag+ was added to the DMSO - HEPES buffer solution (pH = 7). An interference test with other metal ions was determined, and the high selectivity of Hg2+ and Ag+ did not interfere with other metal ions in colorimetric and fluorogenic methods. The possible mechanism of binding of these metal ions and the probe L 1:1 complex was determined by H1 NMR. Additionally, the reversibility of the affinity of probe L with mercury (Hg2+) and silver (Ag+) ions was investigated by adding Na2EDTA. The naked eye detected the "Off-On" type fluorescence sensor in the presence of Hg2+ and EDTA. The tested test strip kits provided a strong probability of probe L with high response and rapid, sensitive detection with Hg2+ ion, which may be suitable for practical use.
ABSTRACT
Follicular maturation arrest is a prevalent endocrine disorder characterized by hormonal imbalance, ovarian dysfunction, and metabolic disturbances leading to Polycystic ovarian syndrome (PCOS). Tanshinone IIA (TIIA), a bioactive compound derived from Salvia miltiorrhiza, has shown promising therapeutic potential in various diseases, including cardiovascular diseases and cancer. However, its effects on reproductive health and gynecological disorders, particularly PCOS, remain poorly understood. In this study, we investigated the potential therapeutic effects of TIIA on ovarian function. Using a combination of experimental and computational approaches, we elucidated the molecular mechanisms underlying TIIA's pharmacological impact on ovarian function, follicular development, and androgen receptor signaling. Molecular docking and dynamics simulations revealed that TIIA interacts with the human androgen receptor (HAR), modulating its activity and downstream signaling pathways. Our results demonstrate that TIIA treatment alleviates PCOS-like symptoms in a zebrafish model, including improved follicular development, lowered GSI index, improved antioxidant status (SOD, CAT), decreased LDH levels, and enhanced AChE levels by regulating Tox3 and Dennd1a pathway. Our findings suggest that TIIA may hold promise as a novel therapeutic agent for the management of PCOS or ovulation induction.
Subject(s)
Abietanes , Ovarian Follicle , Polycystic Ovary Syndrome , Receptors, Androgen , Salvia miltiorrhiza , Zebrafish , Animals , Humans , Abietanes/pharmacology , Receptors, Androgen/metabolism , Salvia miltiorrhiza/chemistry , Polycystic Ovary Syndrome/drug therapy , Polycystic Ovary Syndrome/metabolism , Polycystic Ovary Syndrome/pathology , Ovarian Follicle/drug effects , Ovarian Follicle/metabolism , Ovarian Follicle/pathology , Female , Molecular Docking Simulation , Zebrafish Proteins/metabolism , Signal Transduction/drug effects , Protein Binding/drug effectsABSTRACT
BACKGROUND AND PURPOSE: Parkinson's disease (PD) is a prevalent neurodegenerative movement disorder characterized by motor dysfunction. Environmental factors, especially manganese (Mn), contribute significantly to PD. Existing therapies are focused on motor coordination, whereas nonmotor features such as neuropsychiatric symptoms are often neglected. Daidzein (DZ), a phytoestrogen, has piqued interest due to its antioxidant, anti-inflammatory, and anxiolytic properties. Therefore, we anticipate that DZ might be an effective drug to alleviate the nonmotor symptoms of Mn-induced Parkinsonism. EXPERIMENTAL APPROACH: Naïve zebrafish were exposed to 2 mM of Mn for 21 days and intervened with DZ. Nonmotor symptoms such as anxiety, social behaviour, and olfactory function were assessed. Acetylcholinesterase (AChE) activity and antioxidant enzyme status were measured from brain tissue through biochemical assays. Dopamine levels and histology were performed to elucidate neuroprotective mechanism of DZ. KEY RESULTS: DZ exhibited anxiolytic effects in a novel environment and also improved intra and inter fish social behaviour. DZ improved the olfactory function and response to amino acid stimuli in Mn-induced Parkinsonism. DZ reduced brain oxidative stress and AChE activity and prevented neuronal damage. DZ increased DA level in the brain, collectively contributing to neuroprotection. CONCLUSION AND IMPLICATIONS: DZ demonstrated a promising effect on alleviating nonmotor symptoms such as anxiety and olfactory dysfunction, through the mitigation of cellular damage. These findings underscore the therapeutic potential of DZ in addressing nonmotor neurotoxicity induced by heavy metals, particularly in the context of Mn-induced Parkinsonism.
Subject(s)
Behavior, Animal , Disease Models, Animal , Isoflavones , Manganese , Parkinsonian Disorders , Zebrafish , Animals , Isoflavones/pharmacology , Isoflavones/therapeutic use , Behavior, Animal/drug effects , Manganese/toxicity , Parkinsonian Disorders/drug therapy , Parkinsonian Disorders/chemically induced , Parkinsonian Disorders/metabolism , Acetylcholinesterase/metabolism , Dopamine/metabolism , Oxidative Stress/drug effects , Brain/drug effects , Brain/metabolism , Neuroprotective Agents/pharmacology , Male , Anxiety/drug therapy , Anxiety/chemically induced , Social BehaviorABSTRACT
In this study, we investigated the possible ecotoxicological effect of co-exposure to polystyrene nanoplastics (PS-NPs) and diclofenac (DCF) in zebrafish (Danio rerio). After six days of exposure, we noticed that the co-exposure to PS-NP (100 µg/L) and DCF (at 50 and 500 µg/L) decreased the hatching rate and increased the mortality rate compared to the control group. Furthermore, we noted that larvae exposed to combined pollutants showed a higher frequency of morphological abnormalities and increased oxidative stress, apoptosis, and lipid peroxidation. In adults, superoxide dismutase and catalase activities were also impaired in the intestine, and the co-exposure groups showed more histopathological alterations. Furthermore, the TNF-α, COX-2, and IL-1ß expressions were significantly upregulated in the adult zebrafish co-exposed to pollutants. Based on these findings, the co-exposure to PS-NPs and DCF has shown an adverse effect on the intestinal region, supporting the notion that PS-NPs synergistically exacerbate DCF toxicity in zebrafish.
Subject(s)
Diclofenac , Embryonic Development , Oxidative Stress , Polystyrenes , Water Pollutants, Chemical , Zebrafish , Animals , Zebrafish/embryology , Diclofenac/toxicity , Polystyrenes/toxicity , Water Pollutants, Chemical/toxicity , Embryonic Development/drug effects , Oxidative Stress/drug effects , Embryo, Nonmammalian/drug effects , Nanoparticles/toxicity , Microplastics/toxicity , Drug SynergismABSTRACT
BACKGROUND: Cadmium (Cd) is a hazardous heavy metal that adversely affects the vital body organs particularly liver. Eriocitrin (ERCN) is a plant-based flavonoid that is well-known for its wide range of pharmacological potential. This research trial was aimed to determine the ameliorative potential of ERCN against Cd provoked hepatotoxicity in rats. METHODOLOGY: Twenty-four rats (Rattus norvegicus) were apportioned into control, Cd treated (5â¯mg/kg), Cd (5â¯mg/kg) + ERCN (25â¯mg/kg) and only ERCN (25â¯mg/kg) administrated group. Expressions of Nrf2/Keap1 pathway and apoptotic markers were assessed through qRT-PCR. The levels of inflammatory and liver function markers were evaluated by using standard ELISA kits. KEY FINDINGS: Cd exposure reduced the expression of Nrf2 and anti-oxidant genes as well as the activity of catalase (CAT), glutathione reductase (GSR), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione S-transferase (GST) and glutathione (GSH) contents while escalating the expression of Keap1. Furthermore, Cd intoxication augmented malondialdehyde (MDA) and reactive oxygen species (ROS) levels in hepatic tissues. Exposure to Cd resulted in a notable elevation in the levels of alanine transaminase (ALT), alkaline phosphatase (ALP) and aspartate aminotransferase (AST). Cd administration upregulated nuclear factor-kappa B (NF-κB), interleukin-1 beta (IL-1ß), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) levels as well as cyclooxygenase-2 (COX-2) activity. Furthermore, Cd administration upsurged Bax and Caspase-3 expression while reducing the expression of Bcl-2. Moreover, Cd intoxication disrupted the normal architecture of hepatic tissues. However, supplementation of ERCN significantly (p < 0.05) ameliorated the aforementioned disruptions induced by Cd intoxication. CONCLUSION: ERCN treatment remarkably ameliorated the hepatic tissues owing to its antioxidant, anti-inflammatory, and anti-apoptotic potentials. These findings underscore the therapeutic potential of ERCN to counteract the adverse effects of environmental pollutants on hepatic tissues.
Subject(s)
Cadmium , Kelch-Like ECH-Associated Protein 1 , NF-E2-Related Factor 2 , Animals , Cadmium/toxicity , NF-E2-Related Factor 2/metabolism , Rats , Kelch-Like ECH-Associated Protein 1/metabolism , Male , Liver/drug effects , Liver/metabolism , Chemical and Drug Induced Liver Injury/metabolism , Chemical and Drug Induced Liver Injury/drug therapy , Oxidative Stress/drug effects , Antioxidants/pharmacology , Antioxidants/metabolism , Rats, WistarABSTRACT
Human Carbonic anhydrase IX (hCA IX) is found to be an essential biomarker for the treatment of hypoxic tumors in both the early and metastatic stages of cancer. Due to its active function in maintaining pH levels and overexpression in hypoxic conditions, hCA IX inhibitors can be a potential candidate specifically designed to target cancer development at various stages. In search of selective hCA IX inhibitors, we developed a pharmacophore model from the existing natural product inhibitors with IC50 values less than 50â¯nm. The identified hit molecules were then investigated on protein-ligand interactions using molecular docking experiments followed by molecular dynamics simulations. Among the zinc database 186 hits with an RMSD value less than 1 were obtained, indicating good contact with key residues HIS94, HIS96, HIS119, THR199, and ZN301 required for optimum activity. The top three compounds were subjected to molecular dynamics simulations for 100â¯ns to know the protein-ligand complex stability. Based on the obtained MD simulation results, binding free energies are calculated. Density Functional Theory (DFT) studies confirmed the energy variation between the Highest Occupied Molecular Orbital (HOMO) and Lowest Unoccupied Molecular Orbital (LUMO). The current study has led to the discovery of lead compounds that show considerable promise as hCA IX inhibitors and suggests that three compounds with special molecular features are more likely to be better-inhibiting hCA IX. Compound S35, characterized by a higher stability margin and a smaller energy gap in quantum studies, is an ideal candidate for selective inhibition of CA IX.
Subject(s)
Antigens, Neoplasm , Carbonic Anhydrase Inhibitors , Density Functional Theory , Molecular Docking Simulation , Molecular Dynamics Simulation , Humans , Antigens, Neoplasm/metabolism , Antigens, Neoplasm/chemistry , Carbonic Anhydrase Inhibitors/chemistry , Carbonic Anhydrase Inhibitors/pharmacology , Ligands , Molecular Structure , PharmacophoreABSTRACT
This study investigates the individual and combined toxic effects of Bisphenol A (BPA) and Cadmium (Cd) in zebrafish, recognizing the complex mixture of pollutants organisms encounter in their natural environment. Examining developmental, neurobehavioral, reproductive, and physiological aspects, the study reveals significant adverse effects, particularly in combined exposures. Zebrafish embryos exposed to BPA + Cd exhibit synergistically increased mortality, delayed hatching, and morphological abnormalities, emphasizing the heightened toxicity of the combination. Prolonged exposure until 10 days post-fertilization underscores enduring effects on embryonic development. BPA and Cd induce oxidative stress, as evidenced by increased production of reactive oxygen species and lipid peroxidation. This oxidative stress disrupts cellular functions, affecting lipid metabolism and immune response. Adult zebrafish exposed to BPA and Cd for 40 days display compromised neurobehavioral functions, altered antioxidant defenses, and increased oxidative stress, suggesting potential neurotoxicity. Additionally, disruptions in ovarian follicle maturation and skeletal abnormalities indicate reproductive and skeletal impacts. Histological analysis reveals significant liver damage, emphasizing the synergistic hepatotoxicity of BPA and Cd. Molecular assessments further demonstrate compromised cellular defense mechanisms, synaptic function, and elevated cellular stress and inflammation-related gene expression in response to combined exposures. Bioaccumulation analysis highlights differential tissue accumulation patterns. In conclusion, this study provides comprehensive insights into the multifaceted toxicological effects of BPA and Cd in zebrafish, raising concerns about potential adverse impacts on environmental ecosystems and human health.
Subject(s)
Cadmium , Phenols , Zebrafish , Humans , Animals , Female , Cadmium/toxicity , Cadmium/metabolism , Zebrafish/physiology , Ecosystem , Benzhydryl Compounds/toxicity , Benzhydryl Compounds/metabolism , Oxidative Stress , HepatocytesABSTRACT
This study investigated the reproductive toxicity of rhodamine B in zebrafish and its transgenerational effects on the F1 generation. In silico toxicity predictions revealed high toxicity of rhodamine B, mainly targeting pathways associated with the reproductive and endocrine systems. In vivo experiments on zebrafish demonstrated that rhodamine B exposure at a concentration of 1.5 mg/L led to significant impairments in fecundity parameters, particularly affecting females. Histopathological analysis revealed distinct changes in reproductive organs, further confirming the reproductive toxicity of rhodamine B, with females being more susceptible than males. Gene expression studies indicated significant suppression of genes crucial for ovulation in rhodamine B-treated female fish, highlighting hormonal imbalance as a potential mechanism of reproductive toxicity. Furthermore, bioaccumulation studies showed the presence of rhodamine B in both adult fish gonads and F1 generation samples, suggesting transgenerational transfer of the dye. Embryotoxicity studies on F1 generation larvae demonstrated reduced survival rates, lower hatching rates, and increased malformations in groups exposed to rhodamine B. Moreover, rhodamine B induced oxidative stress in F1 generation larvae, as evidenced by elevated levels of reactive oxygen species and altered antioxidant enzyme activity. Neurotoxicity assessments revealed reduced acetylcholinesterase activity, indicating potential neurological impairments in F1 generation larvae. Additionally, locomotory defects and skeletal abnormalities were observed in F1 generation larvae exposed to rhodamine B. This study provides comprehensive evidence of the reproductive toxicity of rhodamine B in adult zebrafish and its transgenerational effects on the F1 generation.
Subject(s)
Rhodamines , Water Pollutants, Chemical , Zebrafish , Male , Animals , Female , Zebrafish/metabolism , Acetylcholinesterase/metabolism , Reproduction , Gonads , Water Pollutants, Chemical/metabolismABSTRACT
Epilepsy is a chronic neurological disease characterized by a persistent susceptibility to seizures. Pharmaco-resistant epilepsies, impacting around 30 % of patients, highlight the urgent need for improved treatments. Neuroinflammation, prevalent in epileptogenic brain regions, is a key player in epilepsy, prompting the search for new mechanistic therapies. Hence, in this study, we explored the anti-inflammatory potential of pyrazole benzenesulfonamide derivative (T1) against pentylenetetrazole (PTZ) induced epilepsy-like conditions in in-vivo zebrafish model. The results from the survival assay showed 79.97 ± 6.65 % at 150 µM of T1 compared to PTZ-group. The results from reactive oxygen species (ROS), apoptosis and histology analysis showed that T1 significantly reduces cellular damage due to oxidative stress in PTZ-exposed zebrafish. The gene expression analysis and neutral red assay results demonstrated a notable reduction in the inflammatory response in zebrafish pre-treated with T1. Subsequently, the open field test unveiled the anti-convulsant activity of T1, particularly at a concentration of 150 µM. Moreover, both RT-PCR and immunohistochemistry findings indicated a concentration-dependent potential of T1, which inhibited COX-2 in zebrafish exposed to PTZ. In summary, T1 protected zebrafish against PTZ-induced neuronal damage, and behavioural changes by mitigating the inflammatory response through the inhibition of COX-2.
Subject(s)
Epilepsy , Pentylenetetrazole , Animals , Humans , Zebrafish , Benzenesulfonamides , Cyclooxygenase 2/genetics , Cyclooxygenase 2/metabolism , Epilepsy/chemically induced , Epilepsy/drug therapy , Epilepsy/metabolism , Pyrazoles/pharmacology , Pyrazoles/therapeutic use , Disease Models, AnimalABSTRACT
Indole-3-acetic acid (IAA) is the most widely utilized plant growth regulator. Despite its extensive usage, IAA is often overlooked as an environmental pollutant. Due to its protein-binding nature, it also functions as a uremic toxin, contributing to its association with chronic kidney disease (CKD). While in vitro and epidemiological research have demonstrated this association, the precise impact of IAA on cardiovascular disease in animal models is unknown. The main objective of this study is to conduct a mechanistic analysis of the cardiotoxic effects caused by IAA using male Wistar albino rats as the experimental model. Three different concentrations of IAA (125, 250, 500 mg/kg) were administered for 28 days. The circulating IAA concentration mimicked previously observed levels in CKD patients. The administration of IAA led to a notable augmentation in heart size and heart-to-body weight ratio, indicating cardiac hypertrophy. Echocardiographic assessments supported these observations, revealing myocardial thickening. Biochemical and gene expression analyses further corroborated the cardiotoxic effects of IAA. Dyslipidemia, increased serum c-Troponin-I levels, decreased SOD and CAT levels, and elevated lipid peroxidation in cardiac tissue were identified. Moreover, increased expression of cardiac inflammatory biomarkers, including ANP, BNP, ß-MHC, Col-III, TNF-α, and NF-κB, was also found in the IAA-treated animals. Histopathological analysis confirmed the cardiotoxic nature of IAA, providing additional evidence of its adverse effects on cardiovascular health. These results offer insights into the potential negative impact of IAA on cardiovascular function, and elucidating the underlying mechanisms of its cardiotoxicity.
Subject(s)
Cardiomegaly , Indoleacetic Acids , Rats, Wistar , Animals , Male , Rats , Cardiomegaly/chemically induced , Cardiomegaly/pathology , Oxidative Stress/drug effects , Myocardium/metabolism , Myocardium/pathology , Biomarkers/blood , Lipid Peroxidation/drug effects , CardiotoxicityABSTRACT
Paraprobiotics, known as non-viable or ghost probiotics, have attracted attention for their benefits over live microbial cells. This study was designed to investigate the paraprobiotic effects of heat-killed Bacillus coagulans on the white leg shrimp Litopenaeus vannamei. The paraprobiotic formulation was prepared in three different concentrations including B. coagulans 1 (107 cells g-1 diet), B. coagulans 2 (108 cells g-1 diet), and B. coagulans 3 (109 cells g-1 diet) through heat inactivation method. Preliminary toxicity assessments revealed that post-larvae shrimps (mean weight ± SE: 0.025 ± 0.007 g) treated with B. coagulans 1, 2 and 3 paraprobiotic formulations exhibited no mortality, confirming the non-toxic nature of the formulated diet. In a 90-day feeding trial involving juvenile shrimps (mean weight ± SE: 0.64 ± 0.05 g), growth parameters and feed conversion ratios improved in all experimental groups. Subsequently, these shrimps were challenged with Vibrio parahaemolyticus, revealing that paraprobiotic-fed shrimps exhibited significant survival rate improvements. Oxidative stress-related enzyme activities, such as superoxide dismutase and catalase, increased in paraprobiotic-fed shrimps post-Vibrio challenge, while the challenged control group showed decreased activity (p < 0.001). Nitric oxide levels are also increased in paraprobiotic-treated shrimp, with B. coagulans 3 showing a significant rise in nitric oxide activity (p < 0.001). This study further demonstrated the positive impact of paraprobiotic treatment on digestive enzymes, immune-related parameters (e.g., total hemocyte count, prophenoloxidase, and respiratory burst activity), and overall disease resistance. These findings suggest that B. coagulans paraprobiotics have the potential to enhance antioxidant, antibacterial, and immune-related responses in L. vannamei, making them a valuable addition to shrimp aquaculture.
ABSTRACT
INTRODUCTION: Argulus spp. infestation is a significant challenge for aquaculture, currently, there are no approved medications available to efficiently manage this parasite. Consequently, mechanical removal of parasites using forceps and natural substances like herbs are being explored as alternative treatment methods. Pellitorine (PLE) is a naturally occurring compound found in several plant species. It is classified as an alkaloid and belongs to the class of compounds known as amides. MATERIALS AND METHODS: This study aimed to evaluate the effectiveness of PLE in preventing Argulus spp. infestations in goldfish (Carassius auratus) and to determine the optimal dosage of PLE for the detachment of Argulus spp. RESULTS: The findings of this study revealed that PLE enhanced the immune response of goldfish by promoting superoxide dismutase (SOD) and catalase (CAT) in Argulus-infected goldfish. Additionally, PLE induces reactive oxygen species (ROS) generation and cellular damage in the Argulus. PLE at a dosage of 5 mg/mL was able to detach 80% of the argulus from goldfish within 12 h. Therapeutic index was found to be 5.99, suggesting that PLE is the safest drug. CONCLUSIONS: Therefore, our findings suggest that PLE can be a suitable and effective treatment option for preventing Argulus infestations in goldfish. The results of this study can guide the use of PLE at an optimal dosage to control Argulus infestation in goldfish.
Subject(s)
Antioxidants , Antiparasitic Agents , Arguloida , Fatty Acids, Unsaturated , Fish Diseases , Goldfish , Animals , Goldfish/parasitology , Arguloida/drug effects , Fish Diseases/parasitology , Fish Diseases/drug therapy , Antioxidants/pharmacology , Antiparasitic Agents/pharmacology , Polyunsaturated Alkamides/pharmacology , Reactive Oxygen Species/metabolism , Catalase/metabolism , Superoxide Dismutase/metabolismABSTRACT
This research study was designed with the aim to prepare plant extract-mediated iron oxide nanoparticles (IONPs) and different chemically modified carbon adsorbents from the Parthenium hysterophorus plant and then optimize the carbon adsorbents by evaluating their adsorption applications in wastewater for the selected metal ions like arsenic (As3+), lead (Pb2+), and cadmium (Cd2+). The Fourier transform infrared spectroscopy (FTIR) technique was used to highlight functional groups in plant-mediated IONPs and chemically modified carbon adsorbents. A scanning electron microscopy study was conducted to explain the surface morphology of the adsorbents. Energy-dispersive X-rays was used for elemental analysis and X-ray diffraction for particle size and crystallinity of the adsorbents. From the study, it was found that the best optimum conditions were pH = 5-6, initial concentration of adsorbate of 10 mg/L, dose of adsorbent of 0.01 g, contact time of 90-120 min of adsorbent and adsorbate, and temperature of 25 °C. At optimum conditions, the adsorption capacities of IONPs for arsenic (As) 144.7 mg/g, lead (Pb) 128.01 mg/g, and cadmium (Cd) ions 122.1 mg/g were recorded. The activated carbon at optimum conditions showed adsorption capacities of 46.35 mg/g for As, 121.95 mg/g for Pb, and 113.25 mg/g for Cd ion. At equilibrium, Langmuir, Freundlich Temkin, and Dubinin-Radushkevich isotherms were applied on the experimental adsorption data having the best R2 values (0.973-0.999) by the Langmuir isotherm. High-correlation coefficient R2 values (0.996-0.999) were obtained from the pseudo-second-order for all cases, showing that the adsorption process proceeds through pseudo second-order kinetics. The apparent adsorption energy E value was in the range of 0.24-2.36 kJ/mol. The adsorption capacity of regenerated IONPs for As gradually decreased from 144.8 to 45.67 mg/g, for lead 128.15 to 41.65 mg/g, and cadmium from 122.10 to 31.20 mg/g in 5 consecutive cycles. The study showed that the synthesized IONPs and acid-activated carbon adsorbent were successfully used to remove selected metal ions from wastewater.
ABSTRACT
Paraquat (PQ) is a ubiquitous and water-soluble herbicide which has potential to cause systematic poisoning. PQ intoxication is known to be associated with various clinical complications including hepatotoxicity. Amentoflavone (AMF) is an active phenolic compound that exhibits a broad range of biological as well as pharmacological activities. This study was designed to determine the hepato-protective potential of AMF against PQ instigated hepatotoxicity in rats. Forty-eight rats were distributed into four groups such as control group, PQ-treated group (5 mg/kg), PQ (5 mg/kg) + AMF (40 mg/kg) exposed group and AMF (40 mg/kg) only supplemented group. It was revealed that PQ exposure reduced nuclear factor erythroid 2-related factor 2 (Nrf2) and antioxidative genes expression whereas increase the expression of Kelch-like ECH-associated protein 1(Keap1). Besides, PQ intoxication reduced the activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GSR), glutathione peroxidase (GPx), Heme- oxygenase-1 (HO-1) & glutathione (GSH) content. Furthermore, the levels of reactive oxygen species (ROS) & malondialdehyde (MDA) were increased. In addition, PQ significantly increased the hepatic serum enzymes including alkaline phosphatase (ALP), aspartate transaminase (AST), & alanine transaminase (ALT) along with inflammatory biomarkers levels such as tumor necrosis- α (TNF- α), nuclear factor- κB (NF-κB), interleukin-6 (IL-6), interleukin 1beta (IL-1ß), & cyclooxygenase-2 (COX-2) activity. PQ intoxication increased the expressions of pro-apoptotic markers i.e., Bcl-2-associated X protein (Bax) & Cysteine-aspartic protease-3 (Caspase-3) while reducing the expression of anti-apoptotic protein B-cell lymphoma 2 (Bcl-2). Furthermore, PQ intoxication prompted various histopathological impairments. However, the co-administration of AMF significantly improved the abovementioned hepatic damages induced by PQ. The present study indicated that AMF may be an effective therapeutic candidate to mitigate PQ provoked hepatic impairments due to its anti-apoptotic, antioxidant & anti-inflammatory properties.
Subject(s)
Biflavonoids , Chemical and Drug Induced Liver Injury , Paraquat , Rats , Animals , Paraquat/toxicity , Kelch-Like ECH-Associated Protein 1/metabolism , NF-E2-Related Factor 2/metabolism , Antioxidants/pharmacology , Oxidative Stress , Glutathione/metabolism , NF-kappa B/metabolism , Anti-Inflammatory Agents/pharmacology , Chemical and Drug Induced Liver Injury/drug therapy , Chemical and Drug Induced Liver Injury/prevention & controlABSTRACT
[This retracts the article DOI: 10.7759/cureus.18956.].